Karl A. Meyer
University of Illinois at Chicago
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Featured researches published by Karl A. Meyer.
Experimental Biology and Medicine | 1942
Karl A. Meyer; Hans Popper; Frederick Steigmann; William H. Walters; Sol Zevin
Summary The vitamin A content of biopsy specimens of human livers determined chemically and by fluorescence microscopy was compared with the plasma vitamin A level. No parallelism was found between liver and plasma vitamin A, except that subjects with high blood levels had at least an average liver storage.
American Journal of Surgery | 1946
Karl A. Meyer; Wm.H. Requarth; Donald D. Kozoll
Abstract 1. 1. The mortality rate for the removal of acute non-perforated appendices was well under 1 per cent, without significant improvement in recent years. 2. 2. A lowering of the mortality rate from 26.4 per cent to 13.9 per cent has occurred in the treatment of acute perforated appendices with appendiceal peritonitis; this is attributed chiefly to chemotherapy. 3. 3. The greatest improvement in the treatment of acute appendiceal abscesses occurred from non-operative intervention. 4. 4. The McBurney-McArthur muscle-splitting incision is associated with the lowest mortality rate; the closer the incision is made to the mid-line, the higher the mortality rate. 5. 5. Appendectomy with drainage of the peritoneal cavity was associated with the highest mortality rate. 6. 6. Appendectomy without drainage of the peritoneal cavity showed a much lower mortality rate than similar cases which were drained. 7. 7. Appendectomy with drainage of the wound (usually for a perforated appendix) showed a mortality rate slightly lower than appendectomy without drainage but a much lower incidence of wound infections. 8. 8. The surgical principles thought to be of value in the treatment of acute appendicitis are discussed in full detail.
Gastroenterology | 1949
Mitchell Zweig; Karl A. Meyer; Frederick Steigmann
Summary 1.Protein hydrolysates, administered intravenously, stimulated gastric acidity in 55 per cent of tests performed. 2.Factors influencing the acidity were (a) histamine content, (b) pH of the solution, (c) the nature of the diluent used with the protein hydrolyaste. 3.Protein hydrolysa,tes in 5 percent dextrose solution produced gastric stimulation in less instances than those in distilled water. 4.Gastric motility was unaffected by intravenous administration of protein hydrolysates. 5.Neither vagotomy nor thoracic sympathectomy and splanchnicectomy inhibited the gastric response to parenteral protein hydrolysates. Atropine sulfate in small doses given intravenously did not reduce the gastric acidity stimulated by protein hydrolysate infusion; a larger dose, 1/60 grain, noticeably decreased the acid response. 6.Stimulation of gastric acid formation by intravenously administered protein hydrolysates is probably accomplished through (a) a relatively high histamine content, (b) an acid pH, (c) direct action on the gastric glands by the hydrolysate itself, or by a liberated hormone, or (d) by a combination of the three foregoing factors.
Gastroenterology | 1951
Hyman S. Lans; Irving F. Stein; Karl A. Meyer
Studies by Agren and Lagerlof3 on pancreatic function using intravenous secretin demonstrated that changes in the duodenal biliary pigment concentration might be of use in determining the functional status of the gallbladder. Diamonds, Lakel7 , Snape22 , Dreiling and Hollander9 , have described this biliary pigment response in the secretin test and concluded that good correlation exists between the results of the test and gallbladder function. These workers found that prior to injection of secretin, bile was present in the duodenal contents and that after secretin was injected, all visible evidences of bile disappeared for a variable period of time if a normally functioning gallbladder was present; otherwise the bile color persisted throughout the test period. Tanturi25 , and Still24, have demonstrated that secretin acts directly upon the liver in producing hydrocholeresis. The secretin induced hydrocholeresis tests the capacity of the gallbladder to act as an expansile reservoir. Grossman and co-workers12, have shown that the hydrocholeresis reSUlting from secretin stimulation is less than that resulting from the injection of bile salts. Dr. M. 1. Grossman, suggested to us the use of a bile salt as a means of testing the reservoir capacity of the gallbladder. Sodium dehydrocholate was chosen for use in this study because of its potent hydrocholeretic effect and low toxicity4. 5. ll. 21, even when administered intravenously. Studies by Ivy14, Berman5, Grodinsll, and their associates, have demonstrated that sodium dehydrocholate produced agreater increase in the volume output of bile than did any other agent tested. Clinically, these results have been confirmed in patients with T -tubes. Our previous studies using duodenal intubation, show that an increased volume output of at least 100 per cent over a one-hour period occurs in response to 10 cc of 20 per cent sodium dehydrocholatet intravenously. The peak of this response occurs, on the average, fifteen minutes after injection and an increased flow of bile is noted for at least forty minutes after injection.
JAMA | 1949
Irving F. Stein; Karl A. Meyer
JAMA Internal Medicine | 1943
Hans Popper; Frederick Steigmann; Karl A. Meyer; Sol Zevin
Annals of Surgery | 1952
Hyman S. Lans; Irving F. Stein; Karl A. Meyer
JAMA | 1943
Frederick Steigmann; Hans Popper; Karl A. Meyer
Archives of Surgery | 1943
Karl A. Meyer; Frederick Steigmann; Hans Popper; William H. Walters
Archives of Surgery | 1945
Hans Popper; Bruno W. Volk; Karl A. Meyer; Donald D. Kozoll; Frederick Steigmann